The effect of apoptosis-2 ligand on irradiation-induced apoptosis in lung adenocarcinima H1975 cells resistant to EGFR-TKI
10.3760/cma.j.issn.0254-5098.2016.06.005
- VernacularTitle:凋亡素2配体对射线诱导的肺腺癌H1975细胞凋亡的影响
- Author:
Xiguang LIU
;
Hongjun ZHANG
;
Tingting SONG
;
Jingdong LI
- Publication Type:Journal Article
- Keywords:
Apoptosis-2 ligand;
Apoptosis;
Irradiation;
H1975 cell-line
- From:
Chinese Journal of Radiological Medicine and Protection
2016;36(6):424-429
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate whether the apoptosis-2 ligand (Apo-2L),known as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL),could enhance irradiation-induced apoptosis in lung adenocarcinima H1975 cells that are resistant to the epithelial growth factor receptor (EGFR)-TKI.Methods Adenocarcinima H1975 cells were randomly divided into four groups:the control group,Apo2L group,irradiation group,and both Apo-2L and irradiation group.H1975 cells were pretreated with Apo2L under different concentrations of 200 and 228 ng/ml at 24 h before irradiation with doses of 1,1.5,2,2.5,3,3.5 and 4 Gy.The apoptosis rates of all groups were analyzed by flow cytometry 24 h post-irradiation.The inhibition rates of cell proliferation were measured by the MTT assay.Results MTT assay showed that the Apo-2L treatment significantly inhibited cell proliferation(x2 =136.17,P ＜ 0.05).The apoptosis rates of the four groups were different significantly,and the apoptosis rate of radiation combined with drug group was significantly higher than the other three groups(x2 =78.02,P ＜0.05).Conclusions The Apo-2L could not only inhibit the proliferation but also promote radiation-induced apoptosis of adenocarcinoma H1975 cells.
